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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Curr+Opin+Nephrol+Hypertens
2015 ; 24
(2
): 139-44
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Transforming growth factor beta1 and aldosterone
#MMPMID25587902
Matsuki K
; Hathaway CK
; Chang AS
; Smithies O
; Kakoki M
Curr Opin Nephrol Hypertens
2015[Mar]; 24
(2
): 139-44
PMID25587902
show ga
PURPOSE OF REVIEW: It is well established that blocking the
renin-angiotensin-aldosterone system (RAAS) is effective for the treatment of
cardiovascular and renal complications in hypertension and diabetes mellitus.
Although the induction of transforming growth factor beta1 (TGFbeta1) by
components of the RAAS mediates the hypertrophic and fibrogenic changes in
cardiovascular-renal complications, it is still controversial as to whether
TGFbeta1 can be a target to prevent such complications. Here, we review recent
findings on the role of TGFbeta1 in fluid homeostasis, focusing on the
relationship with aldosterone. RECENT FINDINGS: TGFbeta1 suppresses the adrenal
production of aldosterone and renal tubular sodium reabsorption. We have
generated mice with TGFbeta1 mRNA expression graded in five steps, from 10 to
300% of normal, and found that blood pressure and plasma volume are negatively
regulated by TGFbeta1. Notably, the 10% hypomorph exhibits primary aldosteronism
and sodium and water retention due to markedly impaired urinary excretion of
water and electrolytes. SUMMARY: These results identify TGFbeta signalling as an
important counterregulatory system against aldosterone. Understanding the
molecular mechanisms for the suppressive effects of TGFbeta1 on adrenocortical
and renal function may further our understanding of primary aldosteronism, as
well as assist in the development of novel therapeutic strategies for
hypertension.
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